The findings are remarkable for two reasons. First, they converge with independently gathered data that had identified nonsynonymous variations in the same gene cluster as significantly associated with nicotine dependence.5,6 Second, they are also consistent with two independent genome-wide association studies that point to the same locus as a modulator of susceptibility for lung cancer.7,8 In addition, there may be an element of added interest in that the α3 and α5 genes partially overlap at their 3′ ends in a tail-to-tail configuration (Figure 1a). As these genes are coexpressed in some areas of the central nervous system (for example, striatum, habenula) and periphery (for example, bronchial epithelial cells) (Figure 1b), their natural antisense transcripts could give rise to RNA–RNA duplexes with potential regulatory functions.9
